Activation of β-catenin signaling in aggrecan-expressing cells in temporomandibular joint causes osteoarthritis-like defects

Abstract

Therapies targeting a cartilage-regulating signaling protein could mitigate painful damage inflicted on the jaw by age-related osteoarthritis. Many older individuals experience degeneration of the temporomandibular joint (TMJ), where the upper and lower jaw connect. Researchers led by Di Chen of Rush University Medical School in Chicago, USA, have developed a genetically-modified mouse model that reveals a likely molecular driver for TMJ osteoarthritis. Previous studies have implicated a protein called β-catenin in this process, and Chen’s team generated mice in which β-catenin levels can be selectively boosted in cartilage-forming cells at skeletal joints. This increased β-catenin markedly altered the organization of TMJ cartilage, with decreased cell proliferation and increased cell death. The effects were strikingly similar to human osteoarthritis, and the researchers hypothesize that compounds that counter β-catenin could offer useful treatments for this condition.

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